In rats, giving kisspeptin-10 (a short protein fragment) either through the bloodstream or directly into the brain briefly boosts the activity of oxytocin‑producing cells. This effect depends on nerve signals from the gut and only shows up in the brain during late pregnancy and nursing, suggesting kisspeptin may help trigger the extra oxytocin needed for birth and milk release.

Circulating oxytocin is critical for normal birth and lactation. Oxytocin is synthesised by hypothalamic supraoptic and paraventricular neurons and is released from the posterior pituitary gland into the circulation. Oxytocin secretion depends on action potentials initiated at the cell body, and we have shown that intravenous (IV) administration of kisspeptin-10 transiently increases the firing rate of supraoptic nucleus oxytocin neurons in anaesthetised, non-pregnant, pregnant and lactating rats. This peripheral effect is likely via vagal afferent input, because disruption of vagal afferents prevented the excitation. In our initial studies, intracerebroventricular (icv) administration of kisspeptin-10 did not alter the firing rate of oxytocin neurons in non-pregnant rats. Remarkably, we have now gathered unpublished observations showing that icv kisspeptin-10 transiently excites oxytocin neurons in late pregnancy and during lactation, suggesting that a central kisspeptin excitation of oxytocin neurons emerges at the end of pregnancy, when increased oxytocin secretion is required for delivery of the fetus and for milk let-down after delivery.